The acute abdomen is one of the most concerning presentations encountered in primary care, often posing a significant diagnostic challenge; the location of the pain and medical history are key to formulating an efficient and effective differential diagnosis.
In this patient's case, the possibilities which immediately leap out are an acute coronary syndrome (ACS), a recurrent episode of acute pancreatitis, and acute cholecystitis. Perforation of a peptic ulcer should also be considered, although this is clinically less likely in the absence of dyspeptic symptoms.
His examination is unremarkable, except for mild epigastric tenderness, which is a nonspecific finding in this context. Thus, further evaluation via basic laboratory studies, serial ECGs, and imaging of the abdomen is an essential next step.
However, serial ECGs turn out to be normal, essentially excluding an ACS. Furthermore, his liver profile and pancreatic enzyme levels are normal, making acute pancreatitis clinically les
s likely, while ultrasound studies show no features suggestive of acute cholecystitis.
In fact, the only abnormalities apparent are the leukocytosis in the complete blood count and the markedly elevated random plasma glucose. Could this be a diabetic emergency?
In this context, the most likely emergency would be a hyperosmolar hyperglycemic state (HHS); however, this is not typically associated with abdominal pain, while this patient's blood glucose and calculated serum osmolality (310 mOsm/kg) are both too low to entertain this diagnosis.
Diabetic ketoacidosis (DKA) is the other possibility; this is well known to present with inexplicable abdominal pain, although it is rare (but not unheard of) in type 2 diabetes.
An arterial blood gas assay (ABG) is a simple and rapid method to confirm or exclude this possibility; this reveals a marked metabolic acidosis, lending fuel to the possibility of DKA. Follow-up assessment of serum ketone bodies reveals ketonemia as well, clinching the diagnosis.
It is very important to appreciate that DKA in persons with type 2 diabetes is usually a response to some other underlying insult. Thus, further imaging of the abdomen via contrast computed tomography (CT) to definitively exclude pancreatic and biliary pathology is justifiable.
Continuing the above line of thought, the possibility of occult infection should also be considered; it is rational to commence empirical antibiotic therapy while a further search is made for an infective focus. His immediate management should also include intravenous (IV) rehydration with careful monitoring of electrolytes.
Note that insulin should be withheld until the patient is properly rehydrated, as this alone may resolve the metabolic disturbances. Sodium bicarbonate administration is only indicated if the pH is <6.9.
Diabetic ketoacidosis (DKA) is one of the key diabetic emergencies associated with diabetes mellitus; while classically associated with type 1 diabetes, it has been known to occur in individuals with type 2 diabetes as well.
Population-based studies indicate a global incidence of 4.6 to 8 episodes per 1,000 patients with DM; the condition affects individuals of all ages, although one-third of cases are below the age of 30, possibly because of the younger demographic type 1 diabetes represents.
In these patients, physical or emotional stress stimulates increased secretion of counter-regulatory hormones such as glucagon, epinephrine, and cortisol, which then stimulate gluconeogenesis and glycogenolysis.
This results in hyperglycemia, increased fluid losses in the urine, dehydration, and hypotension. Enhanced lipolysis leads to an increased production of ketones that accumulate rapidly and precipitate metabolic acidosis.
Furthermore, impaired action of insulin leads to diminished potassium uptake by the skeletal muscle. The resultant hyperosmolar state causes an efflux of potassium into the intracellular space, resulting in a reduction of total body potassium by way of intracellular depletion and increased osmotic diuresis.
Infections are the most common precipitating factor; other key precipitants include poor glycemic control, poor nutritional status, and conditions of increased stress such trauma, myocardial infarction, stroke, pancreatitis, shock, pregnancy, or psychosocial stressors.
DKA may be rapid in onset, at times occuring within less than 24 hours. Affected individuals commonly present with polyuria, polydipsia, weight loss, fatigue, dyspnea, vomiting, abdominal pain, Kussmaul's respirations, and polyphagia.
Signs of dehydration and fluid depletion such as dry mucous membranes, hypotension, and tachycardia are also common, while the breath may have a fruity odor as a result of the raised ketone levels. In the latter stages, altered mentation and frank coma may result.
Of particular note is that the body temperature is usually low to normal even in the presence of active signs of infection.
Key investigations include serum glucose levels, hemoglobin A1C, blood urea nitrogen, creatinine, electrolyte levels, serum pH, and ketones. These, along with a urinalysis and estimation of the anion gap, will help to differentiate DKA from other syndromes that present similarly, such as hyperosmolar hyperglycemic states (HHS), or starvation ketosis.
For definitive diagnosis, the following criteria must be fulfilled:
- Plasma glucose levels >250 mg/dL
- An arterial pH of ≤ 7.30
- Serum bicarbonate levels ≤ 18 mEq/L
- An anion gap >10 mEq/L
The presence of serum and urine ketones will further support a diagnosis of DKA; serum beta-hydroxybutyrate levels provide a more accurate assessment of ketosis than ketone levels alone.
DKA requires emergent management, beginning with optimizing hydration and correcting hyperglycemia, ketoacidosis, and electrolyte abnormalities.
The treatment protocol is to first administer an infusion of 1L of normal saline over one hour. Once potassium levels are >3.3 mEq/L, insulin may be added in a bolus of 0.1 U/kg regular insulin followed by a continuous infusion. If potassium levels are still low, intravenous supplementation is warranted.
Note that patients with DKA may have severely depleted potassium stores and failure to restore adequate serum levels can lead to arrhythmias and cardiac arrest. Furthermore, frequent monitoring is essential to prevent hypoglycemia, the most frequent complication encountered with this condition.
Once the patient has been stabilized and is accepting oral feeds, a transition to subcutaneous short-acting insulin and then long-acting insulin can be initiated, along with close monitoring of the blood sugar and regular follow-ups to prevent recurrences.
Mortality is greatest in the first 24 to 48 hours and can be lowered with continued careful monitoring; in particular, cerebral edema due to a rapid reduction of the serum osmolality remains the most common cause of mortality during treatment.
1. Diabetic ketoacidosis (DKA) is a potentially fatal hyperglycemic crisis characterized by the triad of hyperglycemia, acidemia, and ketonemia.
2. DKA is most often precipitated by an infection, but can be caused by any stressful event, including acute coronary syndromes, stroke, an intra-abdominal pathology.
3. The management revolves around fluid replacement with normal saline and continued monitoring of electrolyte levels before the initiation of IV insulin therapy.
4. The mortality of DKA is greatest in the first 24-48 hours of treatment.